The effect of specific amino acid groups on renal hemodynamics was examined in seven healthy young volunteers. Each subject received a 3-h intravenous infusion according to one of the following protocols: study 1, gluconeogenic amino acids (Arg, Gly, Pro, Cys, Met, Ser); study 2, alanine alone; study 3, branched-chain amino acids (BCAA, Leu, Ile, Val); or study 4, 0.9% saline. The rise (40-60% above base line) in total plasma amino acid concentration was similar in studies 1-3; no change was observed in study 4. During study 1, glomerular filtration rate (GFR) rose by 16% (from 98 +/- 6 to 114 +/- 8 ml.1.73 m-2.min-1, P less than 0.01), and renal plasma flow (RPF) rose by 28% (from 496 +/- 47 to 638 +/- 70 ml.1.73 m-2.min-1, P less than 0.01). After alanine (study 2) and BCAA (study 3) infusion, there was a slight, although not significant, rise in GFR and RPF; during saline infusion (study 4), GFR and RPF remained unchanged. Plasma insulin and growth hormone did not change significantly in any study protocol. Plasma glucagon rose significantly by 30% in study 1 (from 117 +/- 10 to 151 +/- 13 pg/ml, P less than 0.05) but did not change in studies 2-4. In summary, infusion of mixed gluconeogenic amino acids increases both GFR and RPF, and neither alanine nor BCAA infusion caused a consistent alteration in renal hemodynamics.
The immediate (1 day, D1) and late (90 days, D90) effects of unilateral nephrectomy on contralateral renal hemodynamics, and the renal handling of electrolytes and water were investigated in the whole animal. The immediate and late ability of the remnant kidney to autoregulate perfusate flow and glomerular filtration rate (GFR) was studied in the isolated perfused kidney of the rat. In the whole animal, in D1 rats as compared to controls, GFR calculated for a single kidney increased from 0.85 ± 0.3 to 1.1 ± 0.2ml/min (p < 0.05). In D90 rats GFR increased further and was similar to prenephrectomy GFR (1.4 ± 0.5 vs. 1.7 ± 0.5 ml/min, p NS). Urinary prostanoid excretion in 24 h, calculated for one kidney, increased by 50–500% in D1 rats, but returned to prenephrectomy values in D90 rats. In the isolated perfused kidney, decreasing perfusion pressure (PP) from 100 to 70mm Hg did not change the renal vascular resistance (RVR) in control and D90 kidneys, but in D1 kidneys RVR decreased from 8.6 ± 1.3 to 7 ± 1.3 mmHg/ml/min (p < 0.05). In D90 kidneys RVR was significantly lower as compared to control and D1 kidneys at all perfusion pressures. Decreasing PP from 100 to 70 mm Hg resulted in a significant decrease in perfusion flow in control, D1 and D90 kidneys, while with the increase in PP from 100 to 130 mm Hg the perfusion flow increased significantly in all three kidney groups. GFR was not influenced by the decrease in PP from 100 to 70 mm Hg in control and Dl kidneys, but in D90 kidneys GFR decreased from 532.7 ± 171.0 to 227.8 ± 70.0 µl/min (p < 0.01). In Dl kidneys, GFR was similar to that of controls at all perfusion pressures, while in D90 kidneys GFR was significantly higher than control or D1 kidneys at all perfusion pressures. These results indicate that: (a) the recovery in GFR observed at 90 days after uninephrectomy is not related to renal prostanoids; (b) the early increase in GFR is due to systemic factors (an increased GFR in Dl in the whole animal, and unchanged GFR in the isolated perfused kidney); (c) the late increase in GFR is due to both systemic and intrarenal factors (an increased GFR in D90 in both, whole animal and isolated perfused kidney); (d) control, D1 and D90 isolated perfused kidneys failed to autoregulate renal perfusate flow, however, control and D1 isolated kidneys autoregulated GFR when PP was lowered from 100 to 70 mm Hg, while D90 kidneys did not, and (e) the remarkable vasodilation found in D90 kidneys may potentially predispose these kidneys to pressure-related damage.
The hypertrophy of the remaining kidney following uninephrectomy (UNx) has been related to an increase in renal insulin growth factor-I (IGF-I) content. However, while the increase in renal IGF-I lasts for only days after UNx, renal hypertrophy continues for months. In the present study we investigated whether IGF-I also plays a role in the late post uninephrectomy growth of the remaining kidney. Renal IGF-I in the remnant kidney was greater than that of control kidneys (78.3 +/- 17.3 vs 56.0 +/- 14.0 pmol g-1; p < 0.05) 3 days after UNx, tended to remain higher 30 days after UNx (83.8 +/- 23.6 vs 57.3 +/- 14.5 pmol g-1; p = 0.07), but was similar to that of the control kidney when examined 60 days after UNx (66.6 +/- 15.6 vs. 70.4 +/- 6.7 pmol g-1). Serum IGF-I in uninephrectomized rats was similar to that of controls 3 days after UNx, started to increase above the control level at day 10 after UNx and remained higher 30 and 60 days after UNx (75.9 +/- 6.9 vs. 48.7 +/- 7.3 nmol l-1 at 30 days, and 81.2 +/- 13.7 vs 52.9 +/- 11.0 nmol l-1 at day 60, p < 0.05 for both). The kidney weight of uninephrectomized rats was higher by 21% than that of controls 3 days after UNx, by 45% 30 days after UNx and by 63% 60 days after UNx (p < 0.05 for all three observations). At the end of the study, the glomerular volume of uninephrectomized rats was higher by 36% than that of the controls (p < 0.05) We suggest that in the rat, while the initial post uninephrectomy hypertrophy of the remnant kidney is associated with and most probably mediated by an increase in renal IGF-I, the hypertrophy that persists in later post UNx periods is associated with and may be mediated by an increase in serum IGF-I.
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